Disease processes connected with a disturbed fat metabolism or an elevated plasma lipid concentration which lead to an abnormal accumulation of lipoproteins, particularly low density lipoproteins, are associated with the development of atherosclerosis (Robin and Angell, Basic Pathology, pps. 271-274, 2nd Ed., 1976) since approximately two-thirds of the total cholesterol is transported in the blood of the normal patient as low density lipoproteins. Thus, a selective separation of beta-lipoproteins or low density lipoproteins (LDL) should result in a consequent decrease in the blood cholesterol level and consequently, a decrease in the threat of the development of atherosclerosis. This is particularly applicable in the case of genetic LDL-receptor defects or defects in the lipid metabolism, particularly familial hypercholestemia type II, which are responsible for an elevated LDL level.
Previous attempts to remove excess LDL from the patient have proven unsatisfactory. For example, a process is described in German Offenlegensschrift DE-OS 31 35 814 according to which the low-density lipoproteins in extra corporeal circulations can be precipitated from human plasma or serum with heparin at acidic pH-levels. This process has a disadvantage in that the heparin level required for this therapeutic treatment is relatively high and thus introduces a risk of hemorrhage. In addition to this, relatively large amounts of the rather expensive heparin, which is not available as a natural product in unlimited quantities, is needed for each treatment.
Thus, there remains a need for a substance that will precipitate LDL without the dangerous side effects or high cost associated with heparin.